Biosensors; noninvasive method in detection of C-reactive protein (CRP).

Early diagnosis of C reactive protein (CRP) is critical to applying effective therapies for related diseases. Diagnostic technology in today's healthcare systems is mostly deployed in central laboratories, involves expensive and time-consuming processes, and is operated by specialized personnel. For example, the enzyme-linked immunosorbent assay (ELISA), considered the gold standard diagnostic method, is labor-intensive and requires complex procedures such as multiple washing and labeling steps. Due to these limitations of current diagnostic techniques, it is difficult for people to regularly monitor their health and ultimately the disease is more likely to be diagnosed at a later stage. The problem is exacerbated for economically disadvantaged people living in underdeveloped countries. To address these challenges in the traditional diagnostic field, point-of-care (POC) biosensors have emerged as a promising alternative. This allows patients to have their health checked regularly at or near their bedside without resorting to laboratory tests. Nanotechnology-based methods such as biosensors have been extensively researched and developed. Among biosensors, there are also label-free biosensors with high sensitivity that do not require complicated procedures and reduce test time. However, some drawbacks such as high cost, bulky size and need for trained personnel to operate have not been improved. In this review article, we provide an overview of routine methods in CRP diagnosis and then introduce biosensors as a modern, advanced alternative to older methods. Readers of this article can learn about biosensing and its benefits while being aware of the limitations of routine methods.

BDNF receptor antagonism during the induction of morphine dependence exacerbates the severity of physical dependence and ameliorates psychological dependence in rats.

This study examined the effects of systemic administration of the TrkB receptor antagonist (ANA-12) during induction of morphine dependence on the severity of physical and psychological dependence and the cerebrospinal fluid (CSF) BDNF levels in morphine-dependent and withdrawn rats. Rats became morphine-dependent by increasing daily doses of morphine for 7 days, along with ANA-12 injection. Then, rats were tested for the severity of physical dependence on morphine (spontaneous withdrawal signs), anxiety-like (the elevated plus maze), depressive-like (sucrose preference test) behaviors after spontaneous morphine withdrawal. Also, the CSF BDNF levels were assessed 2 h after the last dose of morphine and day 13 after morphine withdrawal in morphine-dependent and withdrawn rats. We found that the morphine withdrawal signs were significantly higher in morphine dependent rats receiving ANA-12 on days of 5-7 after morphine withdrawal, also ANA-12 exacerbated overall dependence severity. While, the percentage of time spent in the open arms and sucrose preference were higher in morphine-dependent rats receiving ANA-12 than morphine-dependent rats receiving saline. Also, the ANA-12 injection decreased the CSF BDNF levels following morphine dependence, while increased it after morphine withdrawal. We conclude that the ANA-12 exacerbated the severity of physical morphine dependence but attenuated the anxiety/depressive-like behaviors in morphine-dependent and withdrawn rats. Also, ANA-12 injection was able to reverse the changes in the CSF BDNF levels. Therefore, ANA-12 is not more likely to complete treatment for opiate addiction.